Intracellular Stimulation of Biochemical Control Mechanisms by Low-dose, Low-let Irradiation

Abstract

Non-specific generation of intracellular free radicals in excess of normal levels, e.g. by the acute radiation absorption event in cells, has led to a delayed and temporary inhibition of thymidine kinase. The enzyme activity reaches a minimum at 4 h even after a low-level exposure with full recovery soon thereafter. This process appears to represent a biochemical response to an initial physical event, but must be distinguished from the response of the DNA repair enzyme system. A reduction of cellular thymidine kinase activity is expected to cause a temporary reduction of DNA synthesis and may be of advantage to the cell. Such a response may be regarded as an instance of radiation hormesis in the sense that such a compensatory response to the stimulus of irradiation may confer protection against a repeated increase in free radical concentration whether by renewed radiation exposure or by metabolism in general. An improvement of the efficiency of repair or an increased level of free radical detoxification should be of benefit to both the individual cell and to the organism as a whole.

Potassium-channel activation in response to low doses of gamma-irradiation involves reactive oxygen intermediates in nonexcitatory cells.

“…[3H]thymidine at 2 ACi/ml (20 Ci/mmol; 1 Ci = 37 GBq) (Amersham) for 16-18 hr before whole-cell recording.…”

Radiation induced hormesis and its cytological evaluation in sunnhemp <i>Crotalaria juncea</i> L.

“…Exposure to low doses of ionizing radiation caused a temporary inhibition in DNA synthesis (Feinendengen et al 1987). The transitory cessation of DNA synthesis lengthens the recovery period for the cell and generates free radical scavengers.…”

An Examination of Radiation Hormesis Mechanisms Using a Multistage Carcinogenesis Model

“…A small transient increase in radical concentrations above the normal level in the cell can cause a measurable activation of detoxification mechanisms, which will act on chemically and radiologically induced radicals (UNSCEAR, 1994). Various other studies also report on the induction of antioxidants through radiation (Zamboglou et al, 1981;Feinendegen et al, 1984Feinendegen et al, , 1987Oberley et al, 1987;Summers et al 1989;Akashi et al, 1995;Wong et al, 1996;Hachiya et al, 1997;Kim et al, 1997;Shimizu et al, 1998;Bravard et al, 1999;Morcillo et al, 2000;Guo et al, 2003). Stecca and Gerber (1998) reviewed potential mechanisms of adaptive response including the activation of later genes that can promote production of growth factors and cytokines, trigger DNA repair, and regulate progress through the cell cycle.…”

“…The evidence for and against hormesis has been summarized in several recent articles in Science (Kaiser, 2003a(Kaiser, , 2003b and Scientific American (Renner, 2003). Feinendegen et al (1987Feinendegen et al ( , 1988 and Bond et al (1987) provided several explanations for the possible existence of radiation hormesis phenomena. They stated that, in the low-dose region, radiation exerts protection against other challenges involving radicals and thus causes a net beneficial effect by temporarily shielding the hit cell against radicals produced through endogenous processes .…”